Our results showed that in BLM-induced pulmonary fibrosis in mice, FAK was activated by binding to the integrin of extracellular matrix protein, resulting in an increase in the phosphorylation of Tyr397 of FAK, followed by activation of pathways, including ERK1/2, and an elevation in the level of p-FAK and p-ERK protein was found. This evidence concerns the gene MAPK1 and pulmonary fibrosis.